Intracellular triglycerides in cardiomyocyte lipid droplets (IMCL)

Intracellular triglycerides in cardiomyocyte lipid droplets serve as a dynamic reservoir of fatty acids, which are the heart's primary fuel source [1]. These droplets are specialized organelles that sequester neutral lipids, protecting the cell from the lipotoxic effects of free fatty acids and their intermediates, such as ceramide and diacylglycerol [2]. However, in pathological states like obesity and diabetes, an oversupply of lipids leads to excessive accumulation, or cardiac steatosis, which is linked to mitochondrial dysfunction, oxidative stress, and impaired contractile function [3]. While not a direct protein target for drug binding, managing these lipid stores is a key therapeutic goal in treating metabolic heart disease [4]. Pharmacological interventions typically aim to enhance fatty acid oxidation or modulate lipolysis through upstream regulators like PPAR-alpha or SGLT2 inhibitors to restore lipid homeostasis and prevent heart failure progression [5]. Non-invasive monitoring of these lipid levels is often achieved using proton magnetic resonance spectroscopy (1H-MRS) [6]. Sources: [1] Schulze PC, et al. "Lipid accumulation and heart failure." (PubMed) [2] Goldberg IJ, et al. "Lipid droplets in the heart." (PMC4914033) [3] Sharma S, et al. "Intramyocardial lipid accumulation in the failing human heart." (PubMed 15105334) [4] McGavock JM, et al. "Cardiac steatosis in diabetes." (PubMed 17327425) [5] Verma S, et al. "SGLT2 inhibitors and cardiac metabolism." (PubMed 29305103) [6] Szczepaniak LS, et al. "Myocardial triglycerides and 1H-MRS." (PubMed 12606571)

Other names

Myocardial triglyceridesIntramyocardial lipid contentCardiac lipid dropletsMyocardial lipid droplets

Modulation of lipid metabolism through activation of fatty acid oxidation and reduction of lipogenesis via upstream regulatory pathways.